ArticleEvidence-based complementary and alternative medicine : eCAM2014
Ethyl Acetate Extract of Artemisia anomala S. Moore Displays Potent Anti-Inflammatory Effect.
Article in Evidence-based complementary and alternative medicine : eCAM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Mechanisms shaping the role of ERK1/2 in cellular senescence (Review).Molecular medicine reports · 2019Review
- Ethyl Acetate Fraction fromEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Evaluation of potential anti-toxoplasmosis efficiency of combined traditional herbs in a mouse model.Journal of Zhejiang University. Science. B · 2017Article
- The Anti-Inflammatory Effects of a Yin Zhi Huang Soup in an Experimental Autoimmune Prostatitis Rat Model.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Application of Partial Internal Transcribed Spacer Sequences for the Discrimination of Artemisia capillaris from Other Artemisia Species.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- The Nociceptive and Anti-Inflammatory Effects of Artemisia dracunculus L. Aqueous Extract on Fructose Fed Male Rats.Evidence-based complementary and alternative medicine : eCAM · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Artemisia anomala S. Moore has been widely used in China to treat inflammatory diseases for hundreds of years. However, mechanisms associated with its anti-inflammatory effect are not clear. In this study, we prepared ethyl acetate, petroleum ether, n-BuOH, and aqueous extracts from ethanol extract of Artemisia anomala S. Moore. Comparing anti-inflammatory effects of these extracts, we found that ethyl acetate extract of this herb (EAFA) exhibited the strongest inhibitory effect on nitric oxide (NO) production in LPS/IFN γ -stimulated RAW264.7 cells. EAFA suppressed the production of NO in a time- and dose-dependent manner without eliciting cytotoxicity to RAW264.7 cells. To understand the molecular mechanism underlying EAFA's anti-inflammatory effect, we showed that EAFA increased total cellular anti-oxidant capacity while reducing the amount of inducible nitric oxide synthase (iNOS) in stimulated RAW264.7 cells. EAFA also suppressed the expression of IL-1 β and IL-6, whereas it elevates the level of heme oxygenase-1. These EAFA-induced events were apparently associated with NF- κ B and MAPK signaling pathways because the DNA binding activity of p50/p65 was impaired and the activities of both ERK and JNK were decreased in EFEA-treated cells comparing to untreated cells. Our findings suggest that EAFA exerts its anti-inflammatory effect by inhibiting the expression of iNOS.
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Registered trials
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